Short-term monocular deprivation effects are widespread in the visual cortex and extend subcortically to the ventral pulvinar, while sparing the dorsal pulvinar and the lateral geniculate nucleus.

Genetic and electrophysiology experiments provide the first direct evidence that protein kinase C is a calcium-sensing protein in post-tetanic potentiation, a form of synaptic plasticity that supports short-term memory.

The interplay of recurrent excitation and short-term plasticity enables nonlinear transient amplification, an ideal mechanism for selective amplification, pattern completion, and pattern separation in recurrent neural networks.

Genetic and electrophysiological experiments define how homeostatic signaling stabilizes both the gain and short-term dynamic properties of neurotransmitter release, ensuring that synaptic information transfer remains robust to external perturbation.

Molecular, structural and functional diversity of cerebellar granule cell inputs on single molecular layer interneurons extends information processing in feed-forward inhibition microcircuits.

The combination of short-term and long-term plasticity enables hippocampus to learn goal-directed paths through replay in a reversed order.

Proteomic and genetic analysis discovers a new cytoskeletal mechanism of presynaptic short-term plasticity common across neuronal cell types.

Two hour deprivation of vision in one eye transiently boosts the representation of the deprived eye (suppressing the non-deprived eye) in adult human V1 and along the ventral pathway.

By facilitating glutamate and BDNF release, presynaptic NMDA receptors may control information transfer from the dentate gyrus to the CA3 area of the hippocampus.

The analytic theory establishes the general principles of synaptic transmission, enables extraction of microscopic parameters of synaptic fusion machinery from experiments, and links molecular constituents to synaptic function.